Correlation but no causation between leaf nitrogen and maximum assimilation: the role of drought and reproduction in gas exchange in an understory tropical plant Miconia ciliata (Melastomataceae).

Alternative hypotheses were tested to explain a previously reported anomaly in the response of leaf photosynthetic capacity at light saturation (A..) in Miconia ciliata to dry-season irrigation. The anomaly is characterized by an abrupt increase in leaf A._ for nonirrigated plants at the onset of the rainy season to values that significantly exceeded corresponding measurements for plants that were irrigated during the previous dry season. Hypothesis I posits that a pulse in leaf nitrogen increases CO2 assimilation in nonirrigated plants at the onset of the wet season and is dampened for irrigated plants; this hypothesis was rejected because, although a wet-season nitrogen pulse did occur, it was identical for both irrigated and nonirrigated plants and was preceded by the increase in assimilation by nonirrigated plants. Hypothesis 2 posits that a reproduction-related, compensatory photosynthetic response occurs in nonirrigated plants following the onset of the wet season and is dampened in irrigated plants; consistent with hypothesis 2, high maximum assimilation rates for control plants in the wet season were significantly correlated with fruiting and flowering, whereas irrigation caused flowering and fruiting in the dry season, spreading M. ciliata reproductive activity in irrigated plants across the entire year

Control of sympathetic vasomotor tone by catecholaminergic C1 neurones of the rostral ventrolateral medulla oblongata

C1 - Journal Articles RefereedAIMS: Increased sympathetic tone in obstructive sleep apnoea results from recurrent episodes of systemic hypoxia and hypercapnia and might be an important contributor to the development of cardiovascular disease. In this study, we re-evaluated the role of a specific population of sympathoexcitatory catecholaminergic C1 neurones of the rostral ventrolateral medulla oblongata in the control of sympathetic vasomotor tone, arterial blood pressure, and hypercapnia-evoked sympathetic and cardiovascular responses. METHODS AND RESULTS: In anaesthetized rats in vivo and perfused rat working heart brainstem preparations in situ, C1 neurones were acutely silenced by application of the insect peptide allatostatin following cell-specific targeting with a lentiviral vector to express the inhibitory Drosophila allatostatin receptor. In anaesthetized rats with denervated peripheral chemoreceptors, acute inhibition of 50% of the C1 neuronal population resulted in ∼50% reduction in renal sympathetic nerve activity and a profound fall in arterial blood pressure (by ∼25 mmHg). However, under these conditions systemic hypercapnia still evoked vigorous sympathetic activation and the slopes of the CO(2)-evoked sympathoexcitatory and cardiovascular responses were not affected by inhibition of C1 neurones. Inhibition of C1 neurones in situ resulted in a reversible fall in perfusion pressure and the amplitude of respiratory-related bursts of thoracic sympathetic nerve activity. CONCLUSION: These data confirm a fundamental physiological role of medullary catecholaminergic C1 neurones in maintaining resting sympathetic vasomotor tone and arterial blood pressure. However, C1 neurones do not appear to mediate sympathoexcitation evoked by central actions of CO(2)

Brainstem Respiratory Oscillators Develop Independently of Neuronal Migration Defects in the Wnt/PCP Mouse Mutant looptail

The proper development and maturation of neuronal circuits require precise migration of component neurons from their birthplace (germinal zone) to their final positions. Little is known about the effects of aberrant neuronal position on the functioning of organized neuronal groups, especially in mammals. Here, we investigated the formation and properties of brainstem respiratory neurons in looptail (Lp) mutant mice in which facial motor neurons closely apposed to some respiratory neurons fail to migrate due to loss of function of the Wnt/Planar Cell Polarity (PCP) protein Vangl2. Using calcium imaging and immunostaining on embryonic hindbrain preparations, we found that respiratory neurons constituting the embryonic parafacial oscillator (e-pF) settled at the ventral surface of the medulla in Vangl2Lp/+ and Vangl2Lp/Lp embryos despite the failure of tangential migration of its normally adjacent facial motor nucleus. Anatomically, the e-pF neurons were displaced medially in Lp/+ embryos and rostro-medially Lp/Lp embryos. Pharmacological treatments showed that the e-pF oscillator exhibited characteristic network properties in both Lp/+ and Lp/Lp embryos. Furthermore, using hindbrain slices, we found that the other respiratory oscillator, the preBötzinger complex, was also anatomically and functionally established in Lp mutants. Importantly, the displaced e-pF oscillator established functional connections with the preBötC oscillator in Lp/+ mutants. Our data highlight the robustness of the developmental processes that assemble the neuronal networks mediating an essential physiological function

Toksičnost talija u humanoj populaciji

Thallium is a naturally occurring trace element, widely distributed in the earth’s crust, but at very low concentrations. It does not have a known biological use and does not appear to be an essential element for life. It has been considered one of the most toxic heavy metals. Occasionally, there are reports on thallium poisoning as results of suicide or murder attempt or accident. The main threat to humans is through occupational exposure, environmental contamination, and accumulation in food, mainly in vegetables grown on contaminated soil. Increasing use in emerging new technologies and demanding high-tech industry constantly raise concern about exposure risk to all living organisms. Thallium is considered a cumulative poison that can cause adverse health effects and degenerative changes in many organs. The effects are the most severe in the nervous system. The exact mechanism of thallium toxicity still remains unknown, although impaired glutathione metabolism, oxidative stress, and disruption of potassium-regulated homeostasis may play a role. The lack of data about mutagenic, carcinogenic, or teratogenic effects of thallium compounds in humans calls for further research.Talij je u prirodi široko rasprostranjen teški metal, prisutan u vrlo niskim koncentracijama pa ga stoga ubrajamo u elemente u tragovima. Budući da organizmima nije potreban ni u jednoj razvojnoj fazi, ne ubrajamo ga u grupu esencijalnih elemenata. Talij zbog njegovih svojstava ubrajamo među najtoksičnije teške metale. Povremeno se još uvijek pojavljuju slučajevi u kojima je talij upotrijebljen kao sredstvo za pokušaj ubojstva, odnosno samoubojstva, ali i slučajevi nenamjernog, slučajnog trovanja talijem. U današnje vrijeme potencijalna o asnost od trovanja talijem postoji zbog profesionalne izloženosti, izbijanja ekološke katastrofe ili zbog akumulacije u hranidbenim lancima, uglavnom zbog uzgoja hrane na onečišćenom tlu. Sve češća uporaba talija u visokotehnološkoj industriji kao odgovor na zahtjeve moderne tehnologije neprestano povećava rizik od izloženosti svih živih organizama štetnim utjecajima talija u okolišu. Talij ima izuzetno negativan učinak na različite organske sustave, a osobito na živčani sustav. Mehanizmi toksičnosti talija još uvijek nisu u potpunosti razjašnjeni, premda važnu ulogu imaju poremećaji metabolizma glutationa, oksidativni stres i narušavanje homeostaze posredovane ionima kalija. Nedostatak podataka o mutagenim, kancerogenim ili teratogenim učincima talija i njegovih spojeva u ljudi opravdava buduća istraživanja ovog vrlo toksičnog metala

Toksičnost talija u humanoj populaciji

Thallium is a naturally occurring trace element, widely distributed in the earth’s crust, but at very low concentrations. It does not have a known biological use and does not appear to be an essential element for life. It has been considered one of the most toxic heavy metals. Occasionally, there are reports on thallium poisoning as results of suicide or murder attempt or accident. The main threat to humans is through occupational exposure, environmental contamination, and accumulation in food, mainly in vegetables grown on contaminated soil. Increasing use in emerging new technologies and demanding high-tech industry constantly raise concern about exposure risk to all living organisms. Thallium is considered a cumulative poison that can cause adverse health effects and degenerative changes in many organs. The effects are the most severe in the nervous system. The exact mechanism of thallium toxicity still remains unknown, although impaired glutathione metabolism, oxidative stress, and disruption of potassium-regulated homeostasis may play a role. The lack of data about mutagenic, carcinogenic, or teratogenic effects of thallium compounds in humans calls for further research.Talij je u prirodi široko rasprostranjen teški metal, prisutan u vrlo niskim koncentracijama pa ga stoga ubrajamo u elemente u tragovima. Budući da organizmima nije potreban ni u jednoj razvojnoj fazi, ne ubrajamo ga u grupu esencijalnih elemenata. Talij zbog njegovih svojstava ubrajamo među najtoksičnije teške metale. Povremeno se još uvijek pojavljuju slučajevi u kojima je talij upotrijebljen kao sredstvo za pokušaj ubojstva, odnosno samoubojstva, ali i slučajevi nenamjernog, slučajnog trovanja talijem. U današnje vrijeme potencijalna o asnost od trovanja talijem postoji zbog profesionalne izloženosti, izbijanja ekološke katastrofe ili zbog akumulacije u hranidbenim lancima, uglavnom zbog uzgoja hrane na onečišćenom tlu. Sve češća uporaba talija u visokotehnološkoj industriji kao odgovor na zahtjeve moderne tehnologije neprestano povećava rizik od izloženosti svih živih organizama štetnim utjecajima talija u okolišu. Talij ima izuzetno negativan učinak na različite organske sustave, a osobito na živčani sustav. Mehanizmi toksičnosti talija još uvijek nisu u potpunosti razjašnjeni, premda važnu ulogu imaju poremećaji metabolizma glutationa, oksidativni stres i narušavanje homeostaze posredovane ionima kalija. Nedostatak podataka o mutagenim, kancerogenim ili teratogenim učincima talija i njegovih spojeva u ljudi opravdava buduća istraživanja ovog vrlo toksičnog metala

Electrochemical Nanoprobes for Single-Cell Analysis

The measurement of key molecules in individual cells with minimal disruption to the biological milieu is the next frontier in single-cell analyses. Nanoscale devices are ideal analytical tools because of their small size and their potential for high spatial and temporal resolution recordings. Here, we report the fabrication of disk-shaped carbon nanoelectrodes whose radius can be precisely tuned within the range 5–200 nm. The functionalization of the nanoelectrode with platinum allowed the monitoring of oxygen consumption outside and inside a brain slice. Furthermore, we show that nanoelectrodes of this type can be used to impale individual cells to perform electrochemical measurements within the cell with minimal disruption to cell function. These nanoelectrodes can be fabricated combined with scanning ion conductance microscopy probes, which should allow high resolution electrochemical mapping of species on or in living cells

Proteolysis of proBDNF Is a Key Regulator in the Formation of Memory

It is essential to understand the molecular processes underlying long-term memory to provide therapeutic targets of aberrant memory that produce pathological behaviour in humans. Under conditions of recall, fully-consolidated memories can undergo reconsolidation or extinction. These retrieval-mediated memory processes may rely on distinct molecular processes. The cellular mechanisms initiating the signature molecular events are not known. Using infusions of protein synthesis inhibitors, antisense oligonucleotide targeting brain-derived neurotrophic factor (BDNF) mRNA or tPA-STOP (an inhibitor of the proteolysis of BDNF protein) into the hippocampus of the awake rat, we show that acquisition and extinction of contextual fear memory depended on the increased and decreased proteolysis of proBDNF (precursor BDNF) in the hippocampus, respectively. Conditions of retrieval that are known to initiate the reconsolidation of contextual fear memory, a BDNF-independent memory process, were not correlated with altered proBDNF cleavage. Thus, the processing of BDNF was associated with the acquisition of new information and the updating of information about a salient stimulus. Furthermore, the differential requirement for the processing of proBDNF by tPA in distinct memory processes suggest that the molecular events actively engaged to support the storage and/or the successful retrieval of memory depends on the integration of ongoing experience with past learning

Calmodulin Activation by Calcium Transients in the Postsynaptic Density of Dendritic Spines

The entry of calcium into dendritic spines can trigger a sequence of biochemical reactions that begins with the activation of calmodulin (CaM) and ends with long-term changes to synaptic strengths. The degree of activation of CaM can depend on highly local elevations in the concentration of calcium and the duration of transient increases in calcium concentration. Accurate measurement of these local changes in calcium is difficult because the spaces are so small and the numbers of molecules are so low. We have therefore developed a Monte Carlo model of intracellular calcium dynamics within the spine that included calcium binding proteins, calcium transporters and ion channels activated by voltage and glutamate binding. The model reproduced optical recordings using calcium indicator dyes and showed that without the dye the free intracellular calcium concentration transient was much higher than predicted from the fluorescent signal. Excitatory postsynaptic potentials induced large, long-lasting calcium gradients across the postsynaptic density, which activated CaM. When glutamate was released at the synapse 10 ms before an action potential occurred, simulating activity patterns that strengthen hippocampal synapses, the calcium gradient and activation of CaM in the postsynaptic density were much greater than when the order was reversed, a condition that decreases synaptic strengths, suggesting a possible mechanism underlying the induction of long-term changes in synaptic strength. The spatial and temporal mechanisms for selectivity in CaM activation demonstrated here could be used in other signaling pathways

Inhibition of Soluble Tumor Necrosis Factor Ameliorates Synaptic Alterations and Ca2+ Dysregulation in Aged Rats

The role of tumor necrosis factor α (TNF) in neural function has been investigated extensively in several neurodegenerative conditions, but rarely in brain aging, where cognitive and physiologic changes are milder and more variable. Here, we show that protein levels for TNF receptor 1 (TNFR1) are significantly elevated in the hippocampus relative to TNF receptor 2 (TNFR2) in aged (22 months) but not young adult (6 months) Fischer 344 rats. To determine if altered TNF/TNFR1 interactions contribute to key brain aging biomarkers, aged rats received chronic (4–6 week) intracranial infusions of XPro1595: a soluble dominant negative TNF that preferentially inhibits TNFR1 signaling. Aged rats treated with XPro1595 showed improved Morris Water Maze performance, reduced microglial activation, reduced susceptibility to hippocampal long-term depression, increased protein levels for the GluR1 type glutamate receptor, and lower L-type voltage sensitive Ca2+ channel (VSCC) activity in hippocampal CA1 neurons. The results suggest that diverse functional changes associated with brain aging may arise, in part, from selective alterations in TNF signaling